Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Listeria monocytogenes rhombencephalitis has never been studied in a significant group of patients. We describe 14 adult cases who were seen over a 10-year period. A biphasic illness was characteristic: (1) prodromes (5-15 days) with malaise, fatigue, headache, nausea or vomiting, and fever; (2) cranial nerve palsy with facial palsy, diplopia, dysphagia, dysarthria, usually multiple. Meningism and hemi- or tetraparesis were present in 11 patients and cerebellar dysfunction in 9 patients. In 4 cases, CT showed widening of the brain stem with disappearance of the surrounding cisterns. The cerebrospinal fluid was abnormal in all patients in whom this investigation was done (pleocytosis, elevation in protein content). The patients received antibiotic therapy for 2-6 weeks. In the 9 patients who recovered, the neurological dysfunction improved within 2 days to 1 week of the initiation of therapy. There were 5 deaths. At autopsy in 2 cases, there was severe purulent meningitis and rhombencephalitis with predominantly polymorphonuclear cellular infiltration in 1 case, while numerous microabscesses in the midbrain, pons and medulla were observed in the other. We conclude that L. monocytogenes infection should be considered in patients who develop fever and focal neurological signs particularly localized to the brain stem.
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PMID:Early symptoms and outcome of Listeria monocytogenes rhombencephalitis: 14 adult cases. 849 12

Fabry's disease (FD) is a rare, sex-linked disorder resulting from alpha-galactosidase deficiency. Cerebrovascular complications have been reported in the literature but have not been systematically analyzed. We report 2 patients and review 51 previously reported cases (descriptive meta-analysis) to clarify the clinical, radiologic, and pathologic features. The average age at onset of cerebrovascular symptoms was 33.8 years for hemizygous individuals (n = 43) and 40.3 years of heterozygotes (n = 10). The most frequent symptoms and signs were as follows (in descending order of frequency): hemiparesis, vertigo/dizziness, diplopia, dysarthria, nystagmus, nausea/vomiting, head pain, hemiataxia, and ataxia of gait, in the hemizygote group; and memory loss, dizziness, ataxia, hemiparesis, loss of consciousness and hemisensory symptoms, in the heterozygote group. The vertebrobasilar circulation was symptomatic in 67% of the hemizygotes and 60% of the heterozygotes. Intracerebral hemorrhage was found in 4 patients (3 hemizygotes and 1 heterozygote). Elongated, ectatic, tortuous vertebral and basilar arteries were the most common angiographic and pathologic features. For the hemizygotes, the recurrence rate for cerebrovascular disease was 76% and the death rate was 55%; 86% of the heterozygotes had recurrent cerebrovascular event(s) and 40% died. The cerebrovascular manifestations of FD, in both hemizygotes and heterozygotes, are predominantly due to dilative arteriopathy of the vertebrobasilar circulation, frequently recur, and portend a poor prognosis.
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PMID:Cerebrovascular complications of Fabry's disease. 868 96

Two hundred and thirty-one patients were questioned the day following their cataract surgery to ascertain the incidence of postoperative morbidity. One hundred and nineteen patients received local anaesthesia (LA) and 112 received general anaesthesia (GA). There was a significant difference in the incidence of nausea (21% in GA group, 3% in LA group, p < 0.01), sore throat (41% GA group, 3% LA group, p < 0.01), and bruising of the eye (15% GA group, 39% LA group, p < 0.01). There was no significant difference in the incidence of vomiting, headache, double vision, the severity of postoperative pain, or the need for analgesia. The time before the patients drank and ate postoperatively was significantly shorter in the local anaesthetic group (1.3 h and 1.8 h LA group, 4.1 h and 6.7 h GA group respectively, p < 0.01).
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PMID:Postoperative morbidity following cataract surgery. A comparison of local and general anaesthesia. 903 83

Intracranial mixed germ-cell tumors are rare. We describe the findings from six autopsies of patients with these tumors. The patients were all young at presentation (mean age, 16 years), and five of the six were male. Headache, vomiting, polyuria and diplopia were common symptoms. Radiographic evaluation demonstrated a mass on the midline of the brain. The patients were treated mainly with radiation, but survival (mean, 3.7 years) was not as long as predicted. At autopsy, the tumors occupied most of the ventricular spaces, and ranged from being well-circumscribed to invasive. All tumors contained both germinoma components and nongerminomatous germ-cell tumor components. Because the distribution of these components was not homogenous, at least two sections were necessary for the diagnosis. Immunoreactivity for placental alkaline phosphatase was found in all tumors. Immunostaining for human chorional gonadotropin, alpha-fetoprotein and carcinoembryonic antigen was usually associated with abnormally high serum levels of these tumors markers in life. A number of the cells in both kinds of tumor components expressed proliferating cell nuclear antigen, probably reflecting the intense malignant potential.
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PMID:Mixed germ-cell tumor of the brain. Pathologic study of six autopsy cases. 885 48

A girl with HIV infection acquired at birth by blood transfusion, was admitted at the age of 10 years for diplopia, vomiting, headache and papilledema. CT scan was negative. A lumbar puncture revealed clear CSF, protein 0.40 g/l, glucose 2 mmol/l, 5 mononuclear cells/mm3. The Indian ink preparation and the latex agglutination antigen test were positive for Cryptococcus n. Treatment with amphotericin B and flucytosine was started. After 10 days, since the in vitro susceptibility testing of the isolates showed resistence to both drugs, fluconazolo (400 mg/day) was started. Acetazolamide, furosemide and spironolactone were then added to the antifungal therapy for the persistence of severe intracranial hypertension. Diuretics were maintained for 10 weeks. The patient returned to school two and half months after the admission to the hospital. After 19 months, she is doing well and she is on maintenance of fluconazole (200 mg/day). We hypothesized that the increased intracranial pressure would be due to an impaired CSF reabsorption probably as a consequence of a direct cryptococcal infiltration of the villi.
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PMID:Intracranial hypertension and cryptococcal meningitis in a girl with AIDS. 887 56

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68

Intracranial hypertension is not a definitive diagnosis, but rather a syndrome that may result from a number of neurologic and systemic disorders. Intracranial hypertension refers to prolonged elevation of intracranial pressure, generally above 200 mm H2O. This condition may be recognized by the various clinical signs and symptoms that are manifest in most patients, including headache, papilledema, transient visual obscurations, diplopia, ocular motor disorders, tinnitus, nausea, vomiting, and mental irregularities, as well as dysfunctions of the circulatory and respiratory systems. Thorough medical testing as well as a comprehensive ocular evaluation is indicated in these cases. Intracranial hypertension most commonly results from mass lesions, tension hydrocephalus, and pseudotumor cerebri. Other causes include disorders of venous outflow, such as dural sinus thromboses or arteriovenous malformations, and various encephalopathies. Management for intracranial hypertension may involve medical treatment, drug therapy, or surgical intervention. Typically, diuretics are used initially. Corticosteroids may be used as well, although they are not the first choice for treatment. Cerebrospinal fluid shunting procedures may be necessary if medical treatment fails. Optic nerve sheath decompression may also be attempted when chronic papilledema threatens visual function. It is important that the primary care optometrist recognize the manifestations of intracranial hypertension in order to make necessary referrals for management of the underlying etiologies.
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PMID:Intracranial hypertension. 897 12

A 15-year-old man was admitted because of diplopia and bilateral ptosis which occurred a few days after initial clinical signs, such as fever up, nausea, vomiting and headache. His pupils were anisocoric (Rt. phi 3.5 mm < Lt. phi 6.0 mm). In his left eye, light reflex was absent and its movements were limited in all directions. Brain MRI revealed the findings of paranasal sinusitis in bilateral ethmoidal and sphenoidal sinuses and swelling of bilateral cavernous sinus. Combination of intravenous antibiotic therapy and drainage improved his clinical symptoms and MRI findings. It was diagnosed as the inflammation originated in the sphenoid and ethmoid sinuses, which extended to the cavernous sinus and then involved III, IV, and VI cranial nerves. In conclusion, MRI was very useful to detect the cavernous sinusitis secondary to sphenoidal sinusitis.
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PMID:[A case of paranasal sinusitis-cavernous sinusitis with ophthalmoplegia externa]. 899 45

Idiopathic intracranial hypertension is a disorder of intracerebral pressure regulation and patients run the risk of permanent visual loss. Intracranial hypertension (IH) has been reported rarely in systemic lupus erythematosus (SLE). We reviewed the medical records of 127 patients with lupus nephritis (LN) who were followed up from 1987 to 1996 in our unit. There were six patients with IH which gave a disease prevalence of 4.7% in those with LN. All were females giving a disease prevalence of 5.2% for that sex, a high rate of occurrence of IH in patients with LN. Their age ranged from 22 to 34 y (27.8 +/- 3.6 y). Headache, vomiting and diplopia were the common presenting symptoms and had started 7.3 +/- 4.4 weeks prior to the diagnosis of IH. The cerebrospinal (CSF) opening pressure (413.3 +/- 77.0 mmH2O) was raised in all cases. Biochemical and cytological analyses of CSF were normal. The only abnormal radiological finding was partially empty sella in one patient on magnetic resonance imaging (MRI) (performed in three patients) or computed tomography (CT) (performed in all patients). All patients had serological evidences of active lupus disease at the time of diagnosis of IH. The renal histology was WHO type IV in four cases and III and V in one each indicating severe renal involvement. Laboratory evidences of procoagulant activity were found in the form of positive anticardiolipin antibody (aCL) in two patients, lupus anticoagulant (LA) in two and an otherwise unexplained isolated prolongation of activated partial thromboplastin time (APTT) in the other two. Clinically, one or more episodes of symptomatic venous or arterial thrombosis had occurred in all subjects. In addition to symptomatic measures, all subjects were treated with prednisolone, azathioprine, cyclophosphamide and plasmapheresis according to the protocol of our unit. One patient who did not receive plasmapheresis and cyclophosphamide had a relapse while all others recovered completely. None received anticoagulant therapy. Young females with serologically active lupus, severe forms of renal lesions, past history of venous or arterial thrombosis and laboratory evidences of procoagulant activity, appear to be at increased risk of IH. Thrombotic occlusion of the cerebral arteriolar or venous vascular bed eventually affecting the arachnoid villi and impeding CSF absorption is favoured compared to cerebral venous or sinus thrombosis as the pathogenic mechanism. Combined immunosuppression and plasmapheresis appeared to be beneficial in short and long term follow-up. We propose that patients with SLE and IH have definable risk and pathogenetic factors and are no more to be considered 'idiopathic'. The conditions calls for aggressive intervention which leads to an excellent outcome.
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PMID:Treatable intracranial hypertension in patients with lupus nephritis. 930 63

Two women with hyperemesis gravidarum were first seen with a short history of confusion diplopia, unsteadiness, and fits caused by Wernicke's encephalopathy. The neurologic presentation had been precipitated by a carbohydrate load inadvertently administered without vitamin supplementation. We stress the importance of prescribing thiamine supplements to all women with prolonged vomiting during pregnancy.
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PMID:Two pregnant women with vomiting and fits. 942 66


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